Arrhythmias are variations in heart rate from the normal sinus rate range of approximately 60 to 120 beats per minute (bpm) prevalent in healthy adult humans with normally functioning hearts. In bradycardia, rates are below 60 bpm, whereas in tachycardia, rates are above 120 bpm. Typically, tachycardia results from physical stress (exercise), emotional stress (excitement), consumption of alcoholic or caffeinated beverages, ingestion of certain drugs such as nicotine, and so forth. The heart rate of a healthy person will gradually return to the sinus rate after removal of the tachycardia-inducing factors. Arrhythmias, however, may require special medical treatment. For example, fibrillation is a high rate arrhythmia characterized by completely uncoordinated contractions of sections of conductive cardiac tissue of the affected chamber of the heart, resulting in a complete loss of synchronous contraction of the overall tissue mass. As a consequence, the chamber stops pumping blood effectively and, in the case of ventricular fibrillation, the lack of oxygenated blood in the tissues leads to death within minutes.
Implantation of a cardiac pacemaker has been a typical procedure of choice for treatment of bradycardia patients. The pacemaker is implanted beneath the skin in the patient's chest and delivers electrical impulses to electrodes positioned at the patient's heart, stimulating the heart to beat at a desired rate in the normal sinus range. Cardiac pacing has also been used in the management of tachyarrhythmia. The heart may be artificially stimulated at a faster than normal pacing rate to terminate a tachycardia or to suppress premature atrial or ventricular contractions which could otherwise lead to supra-ventricular or ventricular tachycardia, flutter, or fibrillation. The pulses delivered to the heart for bradycardia or tachycardia therapy need only be of sufficient magnitude to stimulate the excitable myocardial tissue in the immediate vicinity of the pacing electrode.
More recently, the automatic defibrillator has been proposed for implantation in cardiac patients prone to suffer ventricular or tachycardia fibrillation. The device is adapted to shock the heart with electrical pulses of considerably higher energy content than is delivered in pacing pulses. When fibrillation is detected, one or more high energy "counter-shocks" are applied to the heart to overwhelm the chaotic contractions of individual tissue sections and re-establish organized spreading of action potential from cell to cell of the myocardium, thereby restoring the synchronized contraction of the mass of tissue.
To treat bradycardia, tachycardia, or fibrillation, many cardiac stimulators monitor the electrical activity of the heart. The amplitude of electrical events in the heart varies over a wide range, particularly when events in the ventricle, where the "QRS" complex is generated, are compared to events in the atrium, where the "P" complex is produced. Moreover, the onset of tachycardia may be accompanied by a relatively rapid, sustained change in the amplitude of electrical events. It is important, therefore, for the cardiac stimulator to adapt quickly to changing conditions so that the heart's status can be accurately detected. To accomplish this, some form of automatic gain control in the sensing circuits of the implantable heart stimulator should be provided.
A particular system for utilizing automatic gain control and bandpass filtering in a feedback loop for a defibrillator has heretofore been disclosed in U.S. Pat. No. 4,880,004, which is assigned to the same assignee as our present application, and of which one of us is a co-inventor. Another system for a bradycardia or tachycardia pacemaker has been described in U.S. Pat. No. 4,913,145 (also assigned to our assignee).
There remains a continuing need, however, to improve the response characteristics of automatic gain control, so that accurate sensing can be maintained.